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Inflammation plays a pivotal role in the pathophysiology of plaque formation and progression. Optical coherence tomography (OCT) allows high-resolution imaging of tissue microstructure. Intravascular ultrasound (IVUS) has been widely used to serially study plaque progression in relation to various risk factors and medical therapies. The aim of the present study was to investigate the impact of macrophages on lipid rich plaque (LRP) progression.
OCT-derived image was defined as signal-rich distinct confluent punctate regions that exceed the intensity of background speckle noise, which area accompanied by high behind signal attenuation. Other characteristics of OCT were measured and determined. Quantitative IVUS measurements included the lumen cross sectional area (CSA), external elastic membrane (EEM) CSA, and plaque plus media (PM) CSA. The plaque burden was calculated as the PM CSA divided by the lesion EEM CSA multiplied by 100. Distal and proximal reference segments were the most normal-looking cross sections within 10 mm distal and proximal to the lesion site, respectively. The remodeling index was calculated by comparing lesion site EEM CSA to the average of the proximal and distal reference EEM CSA. The total atheroma volume (TAV) was calculated as the sum of PM CSA in all the analyzed frames spaced 1 mm apart. The PAV representing the proportion of the vessel volume occupied by plaque was computed as the percentage of TAV divided by total EEM volume.
We identified 97 lipid-rich plaques (LRP) from 69 statin-naïve patients, who received statin therapy in the following 12 months. The mean age was 55.7±9.4, 43 (62.3%) were male, 34 (49%) had diabetes mellitus, and 44 (64%) had history of hypertension. With statin treatment, the level of low-density lipoprotein cholesterol (LDL-C) was decreased by 25.4% (from 109.4±24.6 mg/dL baseline to 73.9±29.2 mg/dL follow-up, p<0.001). The total cholesterol, triglycerides, and apolipoprotein B were all markedly improved (p<0.001, p<0.001, p<0.001, p=0.005, respectively). Macrophage was observed in 71 LRP, was not observed in 26 LRP without macrophages. OCT and IVUS examinations were conducted at baseline and 12-month follow-up period. The baseline plaque characteristics were similar between LRPs with and without macrophage except for spotty calcification (p=0.005) and microchannel (p=0.008). The fibrous cap thickness (FCT) at 12 months was significantly increased in both groups (LRP with macrophage: 95.6±70.9μm, p<0.001; LRP without macrophage: 120.0±81 μm, p<0.001, respectively) without significant difference between the groups (p=0.169). There is no evident difference in change of OCT-derived lipid arc (-39.0±53.8° vs 34.6±38.6°, p=0.729). No significant change in PAV by IVUS was seen at 12 months in both groups (-0.47±4.3% vs 0.20 ±4.5%, p=0.540).
Statin-induced improvements in lipid rich plaque were not attenuated in lesion with macrophage.